High IFITM3 expression predicts adverse prognosis in acute myeloid leukemia.
Document Type
Article
Publication Date
2-1-2020
Publication Title
Cancer Gene Therapy
Abstract
Acute myeloid leukemia (AML) is a malignancy caused by the uncontrolled and dysregulated clonal expansion of abnormal myeloid primordial cells. In general, the prognosis of AML remains poor despite new discoveries in its pathogenesis and treatment. It is crucial to find early and sensitive biomarkers and continue to explore active targeted treatments. Interferon-induced transmembrane protein (IFITM) family is an important part of the interferon signaling pathway and participate in the regulation of immune cell signaling, adhesion, cancer, and liver cell migration. However, the clinical and prognostic value of the IFITM family in AML has rarely been studied. We screened The Cancer Genome Atlas database and found 155 AML patients with IFITM family (IFITM1-5) expression data. In patients who only received chemotherapy, those with high IFITM3 expression had significantly shorter event-free survival (EFS) and overall survival (OS) than patients with low expression (all P < 0.05). Multivariate analysis demonstrated that high IFITM3 expression was an independent risk factor for EFS and OS in patients only received chemotherapy (all P < 0.05). In patients who underwent allogeneic hematopoietic stem cell transplantation (allo-HSCT), however, all IFITM members had no impact on either EFS or OS. In conclusion, our study elucidated that high IFITM3 expression could be an adverse prognostic factor for AML, whose effect might be overcome by allo-HSCT.
Volume
27
Issue
1-2
First Page
38
Last Page
44
Recommended Citation
Liu Y, Lu R, Cui W, Pang Y, Liu C, Cui L, Qian T, Quan L, Dai Y, Jiao Y, Pan Y, Ye X, Shi J, Cheng Z, Fu L. High IFITM3 expression predicts adverse prognosis in acute myeloid leukemia. Cancer Gene Ther. 2020 Feb;27(1-2):38-44. doi: 10.1038/s41417-019-0093-y. Epub 2019 Mar 29. PMID: 30923336.
DOI
10.1038/s41417-019-0093-y
ISSN
1476-5500
PubMed ID
30923336